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Characterisation of within-host diversity of SARS-CoV-2 provides insights into the mutational and selective mechanisms driving its evolution and has important implications for using within-host variation to inform transmission inference efforts.

Parallel studies in primary human airway cells and stem cell-derived enteroids show that Enterovirus D-68 differentially infects and induces innate immune signaling in the respiratory and intestinal epithelium.

Statistical analysis and LASSO regression modeling provide insights into pathogen-specific host response patterns in cerebrospinal fluid from different disease etiologies to support future classification of pathogen type based on host response patterns in meningitis.

Comprehensive analyses of how mutations in a picornavirus capsid affect viral fitness provide novel insights into viral biology, evolution, and host interactions.

Proteases from diverse viruses, the first described pathogen-encoded activators of human NLRP1, cleave NLRP1 at a sequence that mimics the viral polyprotein, resulting in inflammasome activation and pro-inflammatory cytokine release.

A naturally-occurring small molecule acts as a chemical chaperone in vivo to alter the folding of a budding yeast septin and promote an oligomerization pathway that was lost during evolution.

Genetic and biochemical analyses identify a pathway important for infection by many picornaviruses.

Using a suite of CRISPR technologies, unique chemical tools, and carefully designed biochemical and cell biological assays, we define the mechanism of action of Retro-2, an inhibitor of retrograde toxins.

Quasi-enveloped hepatitis A virions undergo clathrin-mediated endocytosis, followed by ALIX-dependent trafficking to lysosomes where the quasi-envelope is degraded, triggering uncoating of the RNA genome in association with lysosomal membrane rupture.

Rotavirus infection induces phosphorylation and proteasomal degradation of MAVS to suppress host antiviral interferon signaling.